Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lead (Pb) can delay sexual maturation; however, the mechanism and critical time of insult are not clearly defined. Therefore, we assessed maternal Pb levels during low-level gestational and/or lactational exposure, as well as blood and tissue Pb in developing fetuses in relation to the subsequent detrimental effects of Pb on puberty-related hormones and the onset of female puberty. Adult Fisher 344 female rats were gavaged daily with either a 1-ml solution of PbAc containing 12 mg/ml Pb or an equal volume of sodium acetate (NaCl), for the controls, from 30 days prior to breeding until their pups were weaned at 21 days. By cross-fostering at the time of birth, the pups were either exposed to PbAc or NaAc during gestation only, lactation only, or during both gestation and lactation. Pb delayed the timing of puberty and this delay was associated with suppressed serum levels of insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH), and estradiol (E(2)). Liver IGF-1 mRNA was not affected, suggesting that Pb altered translation and/or secretion of IGF-1. We reported previously that peripherally derived IGF-1 acts at the hypothalamic level to facilitate LH release at puberty; hence, we suggest that the action of Pb in decreasing circulating IGF-1 contributes to the delayed puberty. The detrimental effects occurred regardless of the developmental time of exposure, although gestational exposure appeared more sensitive to the effects of Pb. Also, the effects noted were with blood Pb levels less than previously reported and these levels are relevant to human health concerns.
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PMID:Effects of lead (Pb) exposure during gestation and lactation on female pubertal development in the rat. 1222 May 94

The major drug of abuse among teenagers in the United States continues to be ethanol (EtOH), but use is seen in children as young as nine. In the studies reported here, the impact of EtOH on biologic and hormonal parameters of puberty was assessed in female rats. Rats were fed a liquid diet containing EtOH, pair fed an identical liquid diet containing dextrimaltose instead of EtOH, or fed a liquid diet not containing EtOH ad libitum. Feeding was started at 21, 25, or 28 d of age. EtOH markedly delayed the age at vaginal opening (34.5 +/- 0.5 d in controls vs 48.5 +/- 2.4 d in EtOH animals; p < 0.001), delayed the age at first estrous (40.9 +/- 0.6 d in controls vs 61.2 +/- 2.6 d in EtOH animals; p < 0.001), increased the length of the estrous cycle, and decreased the number of proestrous days. EtOH, concomitant with reduced ovarian and uterine weight, decreased serum estradiol and progesterone. Associated with these changes in ovarian hormones there was a selective increase in follicle-stimulating hormone, but not luteinizing hormone. EtOH consistently reduced insulin-like growth factor-1. In general, EtOH-induced disruption was more severe the younger the animals were at the start of feeding. Opiate receptor blockade with naltrexone completely prevented the EtOH-induced delay in vaginal opening. The impact of EtOH on female puberty is dramatic, is an emerging public health problem, and deserves more study.
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PMID:EtOH disrupts female mammalian puberty: age and opiate dependence. 1245 Mar 16

Mild-to-moderate alcohol use has numerous negative consequences for female reproductive function. Animal studies have shown that alcohol consumption disrupts female puberty, and drinking during this period also may affect growth and bone health. Beyond puberty, alcohol has been found to disrupt normal menstrual cycling in female humans and animals and to affect hormonal levels in postmenopausal women. Research has explored the mechanisms of these effects and the implications of these effects for bone health.
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PMID:Alcohol's effects on female reproductive function. 1287 37

The importance of leptin in regulating sexual maturation is supported by data showing that deletions of the leptin gene or alterations in the leptin receptor result in infertility. However, attempts to define a role for leptin in normal puberty have produced equivocal results, leading to the conclusion that, if leptin is involved in puberty, its role is permissive and not obligatory. To better define the importance of leptin in primate puberty, the present study tested the hypothesis that a premature elevation in nocturnal leptin concentrations would accelerate indices of puberty, including nocturnal LH secretion in female rhesus monkeys (Macaca mulatta). Juvenile, gonadally intact females were treated daily with leptin (n = 6; 30 micro g/kg, sc at 1700 h) from 12-30 months of age and were compared with age-matched control females (n = 13). Chronic elevation in peripheral concentrations of leptin increased serum levels of both daytime and nighttime bioactive LH at a significantly younger age compared with control females. The earlier rise in LH in leptin-treated females was associated with an earlier increase in serum estradiol and occurrence of menarche. Despite this effect of leptin, nocturnal serum LH was significantly higher at each age assessed in non-leptin-treated ovariectomized controls (n = 6). In addition, leptin increased skeletal lengths and maturity that were associated with significantly higher serum levels of nocturnal GH and daytime IGF-I. Although body weights were not consistently affected by treatment, body mass index, as an index of body fat, was consistently lower in leptin-treated females. Taken together, these data indicate that the chronic elevation in serum leptin concentrations advances the nocturnal increase in serum LH as well as other parameters of female puberty. Furthermore, the observation that nocturnal LH was higher in age-matched, agonadal females compared with the leptin-treated females suggests that the nongonadal drive to LH secretion is operative in female macaques as early as 14 months of age, suggesting that the effect of leptin on puberty in female primates may involve a diminution in gonadal negative feedback suppression of LH secretion. Such a role would suggest that leptin is permissive yet critical for advancing female puberty.
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PMID:Leptin administration increases nocturnal concentrations of luteinizing hormone and growth hormone in juvenile female rhesus monkeys. 1455 68

The present study was planned to examine the effects of somatic growth on the determination of timing of puberty using Hatano high- and low-avoidance rats (HAAs and LAAs); the rats were genetically selected from Sprague-Dawley (SD) rats for good or poor performance in a two-way active avoidance-learning test. Since these two lines were found to have different characteristics, such as body weight at birth, maternal care and timing of male puberty, the present study characterized female puberty in Hatano rats and then compared postnatal growth and timing of puberty between the two lines of rats when they were nursed by foster SD dams. When nursed under biological dams, HAAs became heavier, exhibited vaginal opening at a younger age and first ovulation was accompanied by more oocytes than LAAs. In all of the HAAs, but none of the LAAs, ovulation was induced by a single s.c. injection of 5 IU equine chorionic gonadotropin (eCG) on day 22 after birth. An additional treatment with 10 IU human CG revealed that, in the ovaries of LAAs, a small number of follicles had developed to an ovulable stage as a result of the treatment. The fostering improved somatic growth, and weights of LAAs were sustained at a heavier level than those of fostered HAAs. The fostering, however, did not eliminate the line difference in the timing of puberty of both sexes; it did accelerate the vaginal opening of LAAs but not the balanopreputial separation. Thus, there is a phenotypic difference in the timing of female puberty in Hatano rats exhibiting a different timing of ovarian development in response to gonadotropin. The present study indicates that postnatal somatic growth is not the predominant determinant in the onset of puberty in Hatano rats.
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PMID:Minor involvement of somatic growth in the onset of puberty of Hatano high- and low-avoidance rats. 1501 58

Several studies suggest an interrelationship between estradiol (E2) and insulin-like growth factor-1 (IGF-1) at the hypothalamic level. The present study was designed to discern if the capability of IGF-1 to release LH and influence the timing of female puberty is influenced by E2. Twenty-eight-day-old female rats were ovariectomized (OVEX), then implanted with a third ventricular (3V) cannula. Two weeks later, these animals received subcutaneous (s.c.) injection of oil, or either one or two injections of E2 in the form of estradiol benzoate (1 microg). Forty-eight hours later, four basal blood samples were drawn then the animals received IGF-1 (200 ng) or saline via the 3V and four more blood samples were taken. Results indicated that E2 replacement lowered basal LH levels and IGF-1 induced a significant LH release in only animals that had E2 levels above 20 pg/ml. These levels of E2 were also associated with increases (p<0.05) in the expression of both IGF-1 receptor (IGF-1R) mRNA and protein. In order to further support the hypothesis that the action of IGF-1 at the time of puberty is influenced by E2, 24-day-old intact female rats received s.c. injection of sesame oil or 0.1 microg of E2. The next day, the E2-treated animals also received twice daily s.c. injections of either IGF-1 (500 ng) or saline until vaginal opening (VO) occurred. The animals that received E2 plus IGF-1 showed VO at 31.1 days, which was 2.5 days earlier (p<0.01) than E2-treated animals and 4 days earlier (p<0.001) than IGF-1-treated and saline control animals. Taken together, these results indicate that the hypothalamic action of IGF-1 to stimulate LH release and advance female pubertal development is dependent upon the influence of E2.
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PMID:Influence of estradiol on insulin-like growth factor-1-induced luteinizing hormone secretion. 1519 71

In recent years, animal models of puberty in children have focused on factors responsible for the developmental increase in gonadotropin secretion independent of gonadal negative feedback. Although the testis may play little if any role in timing the initial increase in gonadotropin secretion in the male, the situation may be different for the female. The present study tested the hypothesis that removal of endogenous estradiol by ovariectomy would produce an immediate increase in nocturnal but not daytime LH and FSH concentrations, an effect reversed by estradiol replacement. Morning (1000 and 1030 h) and evening (2200 and 2230 h) concentrations of bioactive LH and, in selected samples, immunoreactive FSH were evaluated in young juvenile female rhesus monkeys (n = 7) before and after ovariectomy at 13 months of age. Evening but not morning concentrations of gonadotropins were significantly increased within 2 wk of ovariectomy, whereas estradiol replacement returned these to presurgical levels and to those observed in age-matched, gonadally intact females (n = 7). By 145 d after ovariectomy, or approximately 17 months of age, evening as well as morning concentrations of LH were significantly higher than concentrations seen immediately after surgery. Estradiol replacement at approximately 18 months of age suppressed both morning and evening LH but not to the degree seen during a similar treatment after ovariectomy. These data support the hypothesis that, for the female, the developmental rise in diurnal gonadotropin secretion is controlled by a gonad-independent mechanism as well as a gonadal negative feedback inhibition. The importance of gonadal restraint on gonadotropin secretion in young juvenile females is evident only in samples obtained during the evening. These data underscore the notion that, for the female puberty, onset, at least in terms of gonadotropin secretion, is a misnomer and that puberty reflects a progression in multiple control mechanisms that ultimately time the attainment of fertility.
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PMID:Estradiol negative feedback regulates nocturnal luteinizing hormone and follicle-stimulating hormone secretion in prepubertal female rhesus monkeys. 1529 35

Glial erbB-1 and erbB-4 receptors are key components of the process by which neuroendocrine glial cells control LHRH secretion and the onset of female puberty. We now provide evidence that these two signaling systems work in a coordinated fashion to control reproductive function. To generate animals carrying functionally impaired erbB-1 and erbB-4 receptors, we crossed Waved 2 (Wa-2+/+) mice harboring a point mutation of the erbB-1 receptor with mice expressing a dominant-negative erbB-4 receptor in astrocytes. In comparison to single-deficient mice, double-mutant animals exhibited a further delay in the onset of puberty and a strikingly diminished adult reproductive capacity. Ligand-dependent erbB receptor phosphorylation and erbB-mediated MAPK (ERK 1/2) phosphorylation were impaired in mutant astrocytes. Wa-2+/+ or double-mutant astrocytes failed to respond to TGF alpha with production of prostaglandin E2, one of the factors mediating the stimulatory effect of astroglial erbB receptor activation on LHRH release. Medium conditioned by Wa-2+/+ or double-mutant astrocytes treated with TGF alpha failed to stimulate LHRH release from GT1-7 cells. The LH response to ovariectomy was significantly attenuated in mutant mice in comparison with wild-type controls. Although the Wa-2 mutation affects all cells bearing erbB-1 receptors, these results suggest that a major defect underlying the reproductive defects of animals with impaired erbB signaling is a decreased ability of glial cells to stimulate LHRH release. Thus, a coordinated involvement of erbB-1 and erbB-4 signaling systems is required for the normalcy of sexual development and the maintenance of mature female reproductive function.
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PMID:erbB-1 and erbB-4 receptors act in concert to facilitate female sexual development and mature reproductive function. 1559 Nov 45

Research suggests that alcohol consumption during early adolescence may delay the onset of female puberty. Alcohol's effect on sexual development is associated with altered function of insulin-like growth factor 1 (IGF-1). This hormone, which is produced in the liver, travels through the bloodstream to the brain, where it helps coordinate overall physical growth with the maturation of the reproductive system. Long-term alcohol consumption inhibits the production of IGF-1 in the liver. Short-term alcohol administration alters IGF-1 function within the brain, ultimately suppressing the release of specific reproductive hormones that initiate puberty. Large proportions of young girls develop drinking habits that place them at risk for alcohol-related endocrine disorders at a crucial time in female pubertal development.
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PMID:Alcohol's effects on female puberty: the role of insulin-like growth factor 1. 1570 91

Manganese (Mn), an essential element considered important for normal growth and reproduction, has been shown in adults to be detrimental to reproductive function when elevated. Because Mn can cross the blood-brain barrier and accumulate in the hypothalamus, and because it has been suggested that infants and children are potentially more sensitive to Mn than adults, we wanted to determine the effects of Mn exposure on puberty-related hormones and the onset of female puberty. We demonstrated that MnCl(2) when administered acutely into the third ventricle of the brain acts dose-dependently to stimulate luteinizing hormone (LH) release in prepubertal female rats. Incubation of hypothalami in vitro showed that this effect was due to a Mn-induced stimulation of luteinizing hormone releasing hormone (LHRH). Further demonstration that this is a hypothalamic site of action was shown by in vivo blockade of LHRH receptors and lack of a direct pituitary action of Mn to stimulate LH in vitro. To assess potential short-term effects, animals were supplemented with MnCl(2) (10 mg/kg) by gastric gavage from day 12 until day 29, or, in other animals, until vaginal opening (VO). Mn caused elevated serum levels of LH, follicle stimulating hormone, and estradiol, and it initiated a moderate but significant advancement in age at VO. Our results are the first to show that Mn can stimulate specific puberty-related hormones and suggest that it may facilitate the normal onset of puberty. They also suggest that Mn may contribute to precocious puberty if an individual is exposed to elevated levels of Mn too early in development.
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PMID:Manganese acts centrally to stimulate luteinizing hormone secretion: a potential influence on female pubertal development. 1574 10


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